Such non-cell autonomous functions of wild-type p53 are often lost, resulting in a more tumor-permissive microenvironment, when TP53 is deleted or disrupted by nonsense or frameshift mutations, when wild-type p53 is blocked by p53 missense mutants via their dominant-negative effect, and when p53 is degraded by the expression of inhibitors, such as Mdm2 or viral oncoproteins. This evidence concerns the gene TP53 and neoplasm.